Capillary leak syndrome with massive intestinal edema after appendectomy.
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Adult↗
Biomedical subjects
M C Fishbein
Publications and source records attributed to M C Fishbein.
Effect of age on hypertrophy of the rat heart following infarction.
To separate the physiologic process of growth from the pathologic process of hypertrophy in rat hearts with myocardial infarction, we compared 32 young, actively-growing rats (initial age 7 weeks) with 45 mature, slowly-growing rats (initial age 18 weeks). Animals were sacrificed five weeks after induction of infarction. During this period, young animals had a 58% increase in body weight and mature animals an 8% increase (p less than 0.001). Cardiac hypertrophy was directly demonstrated by an increase in cell diameter, in both young and mature animals with more than 15% of the left ventricle infarcted (8.5 +/- 0.8 micron in controls vs. 10.2 +/- 1.4 micron in infarcted rats, p less than 0.01). Hypertrophy was further indicated by constant left ventricular weight despite myocardial loss due to infarction, and by constant viable tissue volume estimate ("remaining myocardial area"). Because of hypertrophy the total amount of remaining myocardial area was constant across subgroups with and without infarction (p greater than 0.2). Therefore, cardiac hypertrophy following infarction in rats is not dependent upon age.
Aging↗
Effects of a positron-emitting vanadium-48 nitinol stent on experimental restenosis in porcine coronary arteries: an injury-response study.
BACKGROUND: The major limitation of coronary stenting is restenosis due to exaggerated neointimal thickening. We evaluated a positron-emitting V48 nitinol stent in a porcine coronary model of restenosis. METHODS AND RESULTS: Pigs (n = 16) received a control nonradioactive and a V48 stent (1.5 or 10.6 muCi) randomized to the left anterior descending artery (LAD) and right coronary artery (RCA). Histology, morphometric variables, and strut injury scores were evaluated after 32 days. Peristrut fibrinoid deposits were greater in the high-dose group (p < 0.0001). Control stent area stenosis (AS) and mean neointimal thickness (NIT) correlated with injury (r = 0.81 and 0.79, respectively). Higher-dose stents reduced AS by 20% (0.57 +/- 0.13 vs. 0.71 +/- 0.16; p = 0.029) and mean NIT by 35% (0.44 +/- 0.16 vs. 0.71 +/- 0.24mm; p = 0.001) compared with controls. Lower-dose 1.5-muCi stents did not differ from controls. NIT over individual struts was reduced in the high-dose group compared with controls by 0.18 mm for grade 1 injury, 0.31 mm for grade 2, and 0.38 mm for grade 3 (p < 0.02 for all comparisons). CONCLUSIONS: 1.5-muCi V48 nitinol stents did not influence vessel histology or restenotic parameters in pig coronary arteries. In contrast, 10.6-muCi stents created a distinctive histological picture consisting of increased fibrinoid deposits on the neointimal-facing side of the struts without cellular organization. Higher dose radioactive stents significantly reduced AS and mean NIT. The reduction in neointimal thickening was greatest when the depth of strut penetration into the vascular wall was most severe.
Alloys↗
Ultrasound angioplasty.
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Angioplasty, Balloon↗
Pathology teach and tell: neonatal Marfan syndrome.
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Female↗
Cytokine expression and endothelial cell and lymphocyte activation in human cardiac allograft rejection: an immunohistochemical study of endomyocardial biopsy samples.
We used monoclonal antibodies and immunohistochemical staining of frozen tissue sections to study the expression of cytokines in human cardiac allograft rejection. The 113 endomyocardial biopsy samples were stained for interleukin (IL)-2, IL-6, and interferon-gamma. The findings were compared to expression of the endothelial cell adhesion molecule ICAM-1, and the lymphocyte receptor for the adhesion molecule VCAM-1, VLA-4. Four biopsy samples from patients with idiopathic cardiomyopathy served as controls. IL-2 was not expressed in lymphocytes of controls and only occasionally in mild or moderate cellular rejection, humoral rejection, and Quilty lesions. IL-2 expression was prominent in severe cellular rejection. Interferon-gamma expression increased in proportion to the severity of cellular rejection and was not expressed in other conditions. IL-6 staining, which was only observed in occasional cases, was mild. Cytokine and adhesion molecule expression tended to increase with the severity of cellular rejection. This study shows that cytokine expression can be documented in human allograft endomyocardial biopsy samples with immunohistochemical techniques. The findings support the concept of an important role for cytokines in human cardiac allograft rejection.
Antigens, CD↗
Expression of cell adhesion molecules in human cardiac allograft rejection.
Adhesion of leukocytes to vascular endothelial cells is a critical step in a variety of inflammatory conditions. We studied the expression and distribution of intercellular adhesion molecule-1 (ICAM-1) and endothelial leukocyte adhesion molecule-1 (ELAM-1) in frozen sections of 83 endomyocardial biopsy specimens from human allograft hearts using monoclonal antibodies and an avidin-biotin complex-alkaline phosphatase staining technique. Cases with cellular or humoral rejection and Quilty lesions were studied. Staining was graded from 0 to 3+ in lymphocytes and in capillary, arterial, venular, and endocardial endothelial cells. Expression of ICAM-1 in capillaries increased with the severity of cellular rejection and was prominent in humoral rejection. ICAM-1 was also expressed in lymphocytes in proportion to the degree of rejection. Little or no ELAM-1 expression was noted. In Quilty lesions the intensity of ICAM-1 expression was similar to that of mild-to-moderate rejection. Thus adhesion molecule expression can be identified in endomyocardial biopsy specimens of patients with rejection, suggesting a role for adhesion molecules in the process of rejection. These findings may prove useful in monitoring rejection and its response to therapy and in developing specific antisera directed against these molecules.
Capillaries↗
Bradyarrhythmias requiring pacemaker implantation after orthotopic heart transplantation: association with rejection.
Patients with severe sinus-node dysfunction that required pacemaker implantation after orthotopic heart transplantation were reviewed. During a 21-month period, 42 transplantations were performed in 41 patients. Five patients (12.2%) required a permanent pacemaker because of severe dysrhythmias. Three patients had moderate-to-severe cellular and/or humoral (vascular) rejection, and two of the five patients (40%) died. In the remaining two patients, bradyarrhythmias were due most likely to trauma to the sinus node during harvesting of the donor heart, and these patients have shown no evidence of significant rejection on repeated biopsies. A strong relationship was found between moderate or severe rejection and the development of significant bradyarrhythmias that required the placement of a permanent pacemaker. The development of severe dysrhythmias during the early or late posttransplantation period should be considered a manifestation of an ongoing rejection episode until proven otherwise. In our experience this evidence of rejection may imply a poor prognostic sign because it is associated with high mortality rates.
Adult↗
Nature and significance of epicardial lymphoid infiltrates in cardiac allografts.
BACKGROUND: Myocardial lymphocytic infiltration after transplantation is usually a manifestation of acute cellular rejection. However, purely endocardial infiltrates are generally not regarded as rejection (so-called "Quilty lesions"). The nature of epicardial lymphoid infiltration in cardiac allografts and its significance when observed in endomyocardial biopsies or autopsies are uncertain. METHODS: Twenty-seven cases of transplant-associated epicardial lymphoid infiltration were identified; 16 cases were identified from 1602 consecutive transplant biopsy specimens from 125 patients, and 11 from 14 autopsies, ranging from 1 to 35 months (mean 7.8 months) after transplantation. RESULTS: The infiltrates were composed of aggregates of lymphocytes and histiocytes distributed throughout the epicardium. Plasma cells were found in 52% of cases, with occasional eosinophils and rare neutrophils. Most were vascular, and four autopsy cases had follicle formation. Twenty-four cases (93%) showed a mixed population of cells in a random distribution consisting of T cells in association with fewer B cells and histiocytes. Fifteen cases (nine autopsies, six biopsies) had acute rejection, and nine autopsies had chronic vascular rejection. Fourteen of twenty-four cases (58%) showed concurrent Quilty lesion (nine autopsies, five biopsies), and the remainder showed at least one Quilty lesion in an earlier biopsy. CONCLUSION: Epicardial lymphoid infiltrates occur with significant frequency after heart transplantation and can be associated with, and mimic, acute cellular rejection. However, they exhibit morphologic and immunophenotypic features which are distinguishable from rejection-associated infiltrates.
B-Lymphocytes↗
Clinical-pathologic features of humoral rejection in cardiac allografts: a study in 81 consecutive patients.
BACKGROUND: Humoral rejection is an infrequently reported, poorly understood form of cardiac allograft rejection. METHODS: We reviewed 81 consecutive heart transplant recipients followed up to 3 years after transplantation to evaluate the frequency and significance of humoral rejection in this population. Histologic features evaluated included capillary endothelial cell swelling, interstitial edema and hemorrhage, and neutrophilic infiltration. Immunofluorescence studies with antibodies to immunoglobulin G, immunoglobulin A, immunoglobulin M, Clq, C'3, HLA-DR, and fibrinogen and immunoperoxidase staining for endothelial cells (factor VIII-related antigen) and macrophages (KP1 [CD68]) were performed. Minimal criteria for the diagnosis of humoral rejection were capillary endothelial cell swelling and any immunoglobulin and complement staining in capillaries. Findings were graded and compared with concurrent hemodynamic measurements. RESULTS: Immunoperoxidase staining showed that most swollen cells in capillaries were macrophages and fewer were endothelial cells. Humoral rejection was detected in 102 biopsy specimens from 42 patients (52%), within 3 weeks of transplantation in 28, and 3 weeks to 4 months later in the other 14 patients. One patient had evidence of humoral rejection almost 3 years after transplantation. A third of biopsy specimens with humoral rejection were associated with abnormal hemodynamics; of these 33 specimens only five had significant (grade 3 or 4) coexisting cellular rejection. Histologic findings most often associated with hemodynamic abnormalities were diffuse capillary endothelial cell swelling and any interstitial hemorrhage or edema. Three patients died of humoral rejection; only 1 had coexisting cellular rejection (grade 3A). CONCLUSIONS: In our experience humoral rejection (1) is not uncommon (52% of patients), (2) is often (33% of cases) associated with hemodynamic abnormalities, and (3) may be fatal.
Biopsy↗
Grade 2 cellular heart rejection: does it exist?
According to the International Society for Heart and Lung Transplantation, a single focus of lymphocytic infiltration associated with myocyte injury in a cardiac allograft endomyocardial biopsy is focal moderate cellular rejection (Grade 2). We reviewed 115 endomyocardial biopsy specimens that were completely negative (n = 17), had a Quilty A (n = 17) or Quilty B (n = 46) lesion, or had a lesion fulfilling the criteria of grade 2 rejection (n = 35). By studying step sections (mean = 18) or sections stained for elastic tissue and collagen, we showed continuity of the focus of grade 2 rejection with the endocardium in 32 of 35 cases; these results justify reclassification of these foci as Quilty B lesions, which are defined as endocardial infiltrates that encroach on the underlying myocardium and that may be associated with myocyte injury but are not generally considered to represent acute rejection. Immunohistochemical staining for T and B lymphocytes and histiocytes showed similar patterns in deeper zones of Quilty B lesions and lesions initially regarded as grade 2 rejection. Normal hemodynamics were observed with 16 of 17 completely negative biopsy specimens, 16 of 17 Quilty A biopsy specimens, 46 of 46 Quilty B biopsy specimens, and 35 of 35 grade 2 rejection biopsy specimens. No grade 2 rejection was treated; only 1 biopsy specimen progressed to grade 3A rejection in a subsequent biopsy 2 months later. Most, if not all, cases of grade 2 cellular rejection can be shown to be Quilty B lesions, are not associated with hemodynamic abnormalities, and do not require augmented immunosuppression.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Pathogenesis of Quilty lesion in cardiac allografts: relationship to reduced endocardial cyclosporine A.
BACKGROUND: Endocardial lymphocytic infiltrates, known as Quilty effect, are a common finding of uncertain pathogenesis in cardiac allografts. Quilty effect was not observed before the use of cyclosporine A for immunosuppression and is not generally regarded as a manifestation of rejection. We hypothesized that the endocardial localization of Quilty effect may be related to a relative absence of cyclosporine A in this region. METHODS: We used an indirect immunofluorescence staining method with rabbit polyclonal anti-cyclosporine A antibodies to detect cyclosporine A in fresh frozen sections of 27 cardiac allograft endomyocardial biopsies. Staining was graded 0 to +3. Negative controls were from untreated transplant candidates and from biopsies with the primary antibody omitted. RESULTS: On comparison of endocardial and myocardial fluorescence in biopsy specimens from patients treated with cyclosporine A, there was less endocardial (0.7 +/- 1.1, p < 0.0001) than myocardial (2.2 +/- 0.5) staining. However, in biopsy specimens with Quilty effect (n = 12), this difference was significantly greater (endocardial = 0.2 +/- 0.6 versus myocardial = 2.3 +/- 0.5; p = 0.005) than in specimens without Quilty effect (n = 10) (endocardial = 1.4 +/- 1.2 versus myocardial = 2.1 +/- 0.6; p = 0.7). Endocardial thickness as measured by ocular micrometry was significantly greater in regions with (32 +/- 19 microns) than without (7 +/- 4 microns) Quilty effect, with involved regions showing increased connective tissue (p < 0.0001). In patients with and without Quilty effect, no differences in donor or recipient demographics, prevalence of diabetes, or plasma cyclosporine A levels were found. CONCLUSIONS: Although it has been postulated that Quilty effect is due to the presence of cyclosporine A in cardiac tissue (toxic effect or immunologic reaction), these data suggest that Quilty effect is related to reduced endocardial presence of cyclosporine A, leading to localized, contained, and usually not clinically significant endocardial rejection.
Adult↗
The stuck catheter: a case report.
Complications after the use of central venous catheters have become more frequent as their use in therapy has increased. As a result, the recognition and management of central venous catheters must be emphasized. We describe a unique problem, that of the "stuck catheter," and its safe and simple solution.
Adult↗